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413 results on '"D’Silva, Nisha J."'

3. Salivary microbiome changes distinguish response to chemoradiotherapy in patients with oral cancer

Author

Medeiros, Marcell Costa de, The, Stephanie, Bellile, Emily, Russo, Nickole, Schmitd, Ligia, Danella, Erika, Singh, Priyanka, Banerjee, Rajat, Bassis, Christine, Murphy, III, George R., Sartor, Maureen A., Lombaert, Isabelle, Schmidt, Thomas M., Eisbruch, Avi, Murdoch-Kinch, Carol Anne, Rozek, Laura, Wolf, Gregory T., Li, Gen, Chen, Grace Y., and D’Silva, Nisha J.

Published
2023
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6. Roadmap for the Emerging Field of Cancer Neuroscience

Author

Monje, Michelle, Borniger, Jeremy C, D’Silva, Nisha J, Deneen, Benjamin, Dirks, Peter B, Fattahi, Faranak, Frenette, Paul S, Garzia, Livia, Gutmann, David H, Hanahan, Douglas, Hervey-Jumper, Shawn L, Hondermarck, Hubert, Hurov, Jonathan B, Kepecs, Adam, Knox, Sarah M, Lloyd, Alison C, Magnon, Claire, Saloman, Jami L, Segal, Rosalind A, Sloan, Erica K, Sun, Xin, Taylor, Michael D, Tracey, Kevin J, Trotman, Lloyd C, Tuveson, David A, Wang, Timothy C, White, Ruth A, and Winkler, Frank

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Neurosciences, Cancer, 2.1 Biological and endogenous factors, Aetiology, Humans, Neoplasms, Nervous System, Biological Sciences, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Mounting evidence indicates that the nervous system plays a central role in cancer pathogenesis. In turn, cancers and cancer therapies can alter nervous system form and function. This Commentary seeks to describe the burgeoning field of "cancer neuroscience" and encourage multidisciplinary collaboration for the study of cancer-nervous system interactions.

Published
2020

32. Supplementary Figure S4 from Increased Nerve Density Adversely Affects Outcome in Oral Cancer

Author

Perez-Pacheco, Cindy, primary, Schmitd, Ligia B., primary, Furgal, Allison, primary, Bellile, Emily L., primary, Liu, Min, primary, Fattah, Aya, primary, Gonzalez-Maldonado, Laura, primary, Unsworth, Shelby P., primary, Wong, Sunny Y., primary, Rozek, Laura S., primary, Rao, Arvind, primary, Wolf, Gregory T., primary, Taylor, Jeremy M.G., primary, Casper, Keith, primary, Mierzwa, Michelle, primary, and D'Silva, Nisha J., primary

Published
2023
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33. Supplementary Table S2 from Increased Nerve Density Adversely Affects Outcome in Oral Cancer

Author

Perez-Pacheco, Cindy, primary, Schmitd, Ligia B., primary, Furgal, Allison, primary, Bellile, Emily L., primary, Liu, Min, primary, Fattah, Aya, primary, Gonzalez-Maldonado, Laura, primary, Unsworth, Shelby P., primary, Wong, Sunny Y., primary, Rozek, Laura S., primary, Rao, Arvind, primary, Wolf, Gregory T., primary, Taylor, Jeremy M.G., primary, Casper, Keith, primary, Mierzwa, Michelle, primary, and D'Silva, Nisha J., primary

Published
2023
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34. Data from Increased Nerve Density Adversely Affects Outcome in Oral Cancer

Author

Perez-Pacheco, Cindy, primary, Schmitd, Ligia B., primary, Furgal, Allison, primary, Bellile, Emily L., primary, Liu, Min, primary, Fattah, Aya, primary, Gonzalez-Maldonado, Laura, primary, Unsworth, Shelby P., primary, Wong, Sunny Y., primary, Rozek, Laura S., primary, Rao, Arvind, primary, Wolf, Gregory T., primary, Taylor, Jeremy M.G., primary, Casper, Keith, primary, Mierzwa, Michelle, primary, and D'Silva, Nisha J., primary

Published
2023
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38. Receptor‐interacting protein (RIP) and Sirtuin‐3 (SIRT3) are on opposite sides of anoikis and tumorigenesis

Author

Kamarajan, Pachiyappan, Alhazzazi, Turki Y, Danciu, Theodora, D'silva, Nisha J, Verdin, Eric, and Kapila, Yvonne L

Subjects
Biomedical and Clinical Sciences, Health Sciences, Public Health, Oncology and Carcinogenesis, Cancer, Digestive Diseases, Dental/Oral and Craniofacial Disease, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Adult, Aged, Anoikis, Carcinoma, Squamous Cell, Cell Line, Tumor, Female, Humans, Male, Middle Aged, Mouth Neoplasms, Receptor-Interacting Protein Serine-Threonine Kinases, Sirtuin 3, sirtuin-3, receptor-interacting protein, anoikis resistance, tumorigenesis, oral squamous cell carcinoma, orasphere, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis, Public health
Abstract

BackgroundRegulating cross-talk between anoikis and survival signaling pathways is crucial to regulating tissue processes and mitigating diseases like cancer. Previously, the authors demonstrated that anoikis activates a signaling pathway involving the CD95/Fas-mediated signaling pathway that is regulated by receptor-interacting protein (RIP), a kinase that shuttles between Fas-mediated cell death and integrin/focal adhesion kinase (FAK)-mediated survival pathways. Because it is known that sirtuin-3 (SIRT3), a nicotinamide adenine dinucleotide-dependent deacetylase, regulates cell survival, metabolism, and tumorigenesis, the authors hypothesized that SIRT3 may engage in cross-talk with Fas/RIP/integrin/FAK survival-death pathways in cancer cell systems.MethodsUsing immunohistochemical staining, immunoblotting, human tissue microarrays, and overexpression and suppression approaches in vitro and in vivo, the roles of RIP and SIRT3 were examined in oral squamous cell carcinoma (OSCC) anoikis resistance and tumorigenesis.ResultsRIP and SIRT3 had opposite expression profiles in OSCC cells and tissues. Stable suppression of RIP enhanced SIRT3 levels, whereas stable suppression of SIRT3 did not impact RIP levels in OSCC cells. The authors observed that, as OSCC cells became anoikis-resistant, they formed multicellular aggregates or oraspheres in suspension conditions, and their expression of SIRT3 increased as their RIP expression decreased. Also, anoikis-resistant OSCC cells with higher SIRT3 and low RIP expression induced an increased tumor burden and incidence in mice, unlike their adherent OSCC cell counterparts. Furthermore, stable suppression of SIRT3 inhibited anoikis resistance and reduced tumor incidence.ConclusionsThe current results indicted that RIP is a likely upstream, negative regulator of SIRT3 in anoikis resistance, and an anoikis-resistant orasphere phenotype defined by higher SIRT3 and low RIP expression contributes to a more aggressive phenotype in OSCC development.

Published
2012

40. Sirtuin‐3 (SIRT3), a novel potential therapeutic target for oral cancer

Author

Alhazzazi, Turki Y, Kamarajan, Pachiyappan, Joo, Nam, Huang, Jing‐Yi, Verdin, Eric, D'Silva, Nisha J, and Kapila, Yvonne L

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Orphan Drug, Digestive Diseases, Dental/Oral and Craniofacial Disease, Cancer, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Animals, Carcinoma, Squamous Cell, Cell Line, Tumor, Cell Proliferation, Cell Survival, Humans, Mice, Mice, Nude, Molecular Targeted Therapy, Mouth Neoplasms, Radiation Tolerance, Sirtuin 3, Up-Regulation, SIRT3, sirtuins, carcinogenesis, oral cancer, squamous cell carcinoma, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis, Public health
Abstract

BackgroundSeveral sirtuin family members (SIRT1-7), which are evolutionarily conserved NAD-dependent deacetylases, play an important role in carcinogenesis. However, their role in oral cancer has not yet been investigated. Therefore, the objective of this study was to investigate whether sirtuins play a role in oral cancer carcinogenesis.MethodsThe expression levels of all sirtuins in several oral squamous cell carcinoma (OSCC) cell lines were compared with normal human oral keratinocytes and observed that SIRT3 was highly expressed. Therefore, tissue microarrays were used to evaluate the clinical relevance of this overexpression. SIRT3 down-regulation in OSCC cell proliferation and survival was investigated and analyzed by using cell-proliferation and cell-viability assays. Ionizing radiation and cisplatin were used to investigate whether SIRT3 down-regulation could increase the sensitivity of OSCC to both treatments. To further assess the in vivo role of SIRT3 in OSCC carcinogenesis, a floor-of-mouth oral cancer murine model was used to study the effect of SIRT3 down-regulation on OSCC tumor growth in immunodeficient mice.ResultsThe current results demonstrated for the first time that SIRT3 is overexpressed in OSCC in vitro and in vivo compared with other sirtuins. Down-regulation of SIRT3 inhibited OSCC cell growth and proliferation and increased OSCC cell sensitivity to radiation and cisplatin treatments in vitro. SIRT3 down-regulation also reduced tumor burden in vivo.ConclusionsThe current investigation revealed a novel role for SIRT3 in oral cancer carcinogenesis as a promoter of cell proliferation and survival, thus implicating SIRT3 as a new potential therapeutic target to treat oral cancer.

Published
2011

41. The CS1 segment of fibronectin is involved in human OSCC pathogenesis by mediating OSCC cell spreading, migration, and invasion

Author

Kamarajan, Pachiyappan, Garcia-Pardo, Angeles, D'Silva, Nisha J, and Kapila, Yvonne L

Subjects
Epidemiology, Biomedical and Clinical Sciences, Health Sciences, Oncology and Carcinogenesis, Cancer, Digestive Diseases, Rare Diseases, Dental/Oral and Craniofacial Disease, 2.1 Biological and endogenous factors, Aetiology, Carcinoma, Squamous Cell, Cell Line, Tumor, Cell Movement, Cell Shape, Fibronectins, Focal Adhesion Kinase 1, Humans, Immunohistochemistry, Integrin alpha4, Intercellular Signaling Peptides and Proteins, Keratinocytes, Mouth Neoplasms, Neoplasm Invasiveness, Neoplasm Staging, Peptides, RNA Interference, Tissue Array Analysis, Transfection, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundThe alternatively spliced V region or type III connecting segment III (IIICS) of fibronectin is important in early development, wound healing, and tumorigenesis, however, its role in oral cancer has not been fully investigated. Thus, we investigated the role of CS-1, a key site within the CSIII region of fibronectin, in human oral squamous cell carcinoma (OSCC).MethodsTo determine the expression of CS-1 in human normal and oral SCC tissue specimens immunohistochemical analyses were performed. The expression of CS1 was then associated with clinicopathological factors. To investigate the role of CS-1 in regulating OSCC cell spreading, migration and invasion, OSCC cells were assayed for spreading and migration in the presence of a CS-1 peptide or a CS-1 blocking peptide, and for invasion using Matrigel supplemented with these peptides. In addition, integrin alpha4siRNA or a focal adhesion kinase (FAK) anti-sense oligonucleotide was transfected into OSCC cells to examine the mechanistic role of integrin alpha4 or FAK in CS1-mediated cell spreading and migration, respectively.ResultsCS-1 expression levels were significantly higher in OSCC tissues compared to normal tissues (p < 0.05). Also, although, high levels of CS-1 expression were present in all OSCC tissue samples, low-grade tumors stained more intensely than high grade tumors. OSCC cell lines also expressed higher levels of CS-1 protein compared to normal human primary oral keratinocytes. There was no significant difference in total fibronectin expression between normal and OSCC tissues and cells. Inclusion of CS-1 in the in vitro assays enhanced OSCC cell spreading, migration and invasion, whereas the CS1 blocking peptide inhibited these processes. Suppression of integrin alpha4 significantly inhibited the CS1-mediated cell spreading. Furthermore, this migration was mediated by focal adhesion kinase (FAK), since FAK suppression significantly blocked the CS1-induced cell migration.ConclusionThese data indicate that the CS-1 site of fibronectin is involved in oral cancer pathogenesis and in regulating OSCC cell spreading, migration and invasion.

Published
2010

42. Oral Microbiome Community Composition in Head and Neck Squamous Cell Carcinoma

Author

Benjamin, William J., primary, Wang, Kai, additional, Zarins, Katherine, additional, Bellile, Emily, additional, Blostein, Freida, additional, Argirion, Ilona, additional, Taylor, Jeremy M. G., additional, D’Silva, Nisha J., additional, Chinn, Steven B., additional, Rifkin, Samara, additional, Sartor, Maureen A., additional, and Rozek, Laura S., additional

Published
2023
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43. Increased Nerve Density Adversely Affects Outcome in Oral Cancer

Author

Perez-Pacheco, Cindy, primary, Schmitd, Ligia B., additional, Furgal, Allison, additional, Bellile, Emily L., additional, Liu, Min, additional, Fattah, Aya, additional, Gonzalez-Maldonado, Laura, additional, Unsworth, Shelby P., additional, Wong, Sunny Y., additional, Rozek, Laura S., additional, Rao, Arvind, additional, Wolf, Gregory T., additional, Taylor, Jeremy M.G., additional, Casper, Keith, additional, Mierzwa, Michelle, additional, and D'Silva, Nisha J., additional

Published
2023
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46. Supplementary Figure 2 from Inactivation or Loss of TTP Promotes Invasion in Head and Neck Cancer via Transcript Stabilization and Secretion of MMP9, MMP2, and IL-6

Author

Van Tubergen, Elizabeth A., primary, Banerjee, Rajat, primary, Liu, Min, primary, Broek, Robert Vander, primary, Light, Emily, primary, Kuo, Shiuhyang, primary, Feinberg, Stephen E., primary, Willis, Amanda L., primary, Wolf, Gregory, primary, Carey, Thomas, primary, Bradford, Carol, primary, Prince, Mark, primary, Worden, Francis P., primary, Kirkwood, Keith L., primary, and D'Silva, Nisha J., primary

Published
2023
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47. Supplementary Figure 3 from Inactivation or Loss of TTP Promotes Invasion in Head and Neck Cancer via Transcript Stabilization and Secretion of MMP9, MMP2, and IL-6

Author

Van Tubergen, Elizabeth A., primary, Banerjee, Rajat, primary, Liu, Min, primary, Broek, Robert Vander, primary, Light, Emily, primary, Kuo, Shiuhyang, primary, Feinberg, Stephen E., primary, Willis, Amanda L., primary, Wolf, Gregory, primary, Carey, Thomas, primary, Bradford, Carol, primary, Prince, Mark, primary, Worden, Francis P., primary, Kirkwood, Keith L., primary, and D'Silva, Nisha J., primary

Published
2023
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48. Supplementary Figure 4 from Inactivation or Loss of TTP Promotes Invasion in Head and Neck Cancer via Transcript Stabilization and Secretion of MMP9, MMP2, and IL-6

Author

Van Tubergen, Elizabeth A., primary, Banerjee, Rajat, primary, Liu, Min, primary, Broek, Robert Vander, primary, Light, Emily, primary, Kuo, Shiuhyang, primary, Feinberg, Stephen E., primary, Willis, Amanda L., primary, Wolf, Gregory, primary, Carey, Thomas, primary, Bradford, Carol, primary, Prince, Mark, primary, Worden, Francis P., primary, Kirkwood, Keith L., primary, and D'Silva, Nisha J., primary

Published
2023
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49. Supplementary Figure 5 from Inactivation or Loss of TTP Promotes Invasion in Head and Neck Cancer via Transcript Stabilization and Secretion of MMP9, MMP2, and IL-6

Author

Van Tubergen, Elizabeth A., primary, Banerjee, Rajat, primary, Liu, Min, primary, Broek, Robert Vander, primary, Light, Emily, primary, Kuo, Shiuhyang, primary, Feinberg, Stephen E., primary, Willis, Amanda L., primary, Wolf, Gregory, primary, Carey, Thomas, primary, Bradford, Carol, primary, Prince, Mark, primary, Worden, Francis P., primary, Kirkwood, Keith L., primary, and D'Silva, Nisha J., primary

Published
2023
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50. Supplementary Methods, Table 1 from Inactivation or Loss of TTP Promotes Invasion in Head and Neck Cancer via Transcript Stabilization and Secretion of MMP9, MMP2, and IL-6

Author

Van Tubergen, Elizabeth A., primary, Banerjee, Rajat, primary, Liu, Min, primary, Broek, Robert Vander, primary, Light, Emily, primary, Kuo, Shiuhyang, primary, Feinberg, Stephen E., primary, Willis, Amanda L., primary, Wolf, Gregory, primary, Carey, Thomas, primary, Bradford, Carol, primary, Prince, Mark, primary, Worden, Francis P., primary, Kirkwood, Keith L., primary, and D'Silva, Nisha J., primary

Published
2023
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